While he is being assessed and resuscitated, an arterial blood gas sample is taken, revealing the following

pH 7.00

PCO2 100

HCO3 - data unavailable

23Case 1

What is the hydrogen ion concentration?

What is the bicarbonate ion concentration?

What is the acid-base disorder?

24Case 1

What is the hydrogen ion concentration?

H 10 (9-pH)

10 (9-7)

10 (2)

100 nEq/L

25Case 1

What is the bicarbonate ion concentration?

Remember that H 24 x (PCO2 / HCO3 - )

Thus,

HCO3 - 24 x (PCO2 / H )

HCO3 - 24 x (100 / 100 )

HCO3 - 24 mEq/L

26Case 1

What is the acid-base disorder?

27Case 1

What is the acid-base disorder?

28Case 1

What is the acid-base disorder?

Recall that for acute respiratory disturbances (where renal compensation does not have much time to occur) each arterial PCO2 shift of 10 mm Hg is accompanied by a pH shift of about 0.08, while for chronic respiratory disturbances (where renal compensation has time to occur) each PCO2 shift of 10 mm Hg is accompanied by a pH shift of about 0.03. 29Case 1

What is the acid-base disorder?

In our case an arterial PCO2 shift of 60 mm Hg (from 40 to 100 mm Hg) is accompanied by a pH shift of 0.40 units (from 7.40 to 7.00), or a 0.067 pH shift for each PCO2 shift of 10 mm. Since 0.067 is reasonably close to the expected value of 0.08 for an acute respiratory disturbance, it is reasonable to say that the patient has an ACUTE RESPIRATORY ACIDOSIS. 30Case 1

Very sick 56 year old man being evaluated for a possible double lung transplant

Dyspnea on minimal exertion

On home oxygen therapy (nasal prongs, 2 lpm)

Numerous pulmonary medications

43

Oxygen therapy via nasal prongs (cannula)

44(No Transcript) 45(No Transcript) 46Case 2

While he is being assessed an arterial blood gas sample is taken, revealing the following

pH 7.30

PCO2 65 mm Hg

47Case 2

What is the hydrogen ion concentration?

What is the bicarbonate ion concentration?

What is the acid-base disorder?

48Case 2

What is the hydrogen ion concentration?

H 10 (9-pH)

10 (9-7.3)

10 (1.7)

50.1 nEq/L

49Case 2

What is the bicarbonate ion concentration?

Remember that H 24 x (PCO2 / HCO3 - )

Thus,

HCO3 - 24 x (PCO2 / H )

HCO3 - 24 x (65 / 50.1 )

HCO3 - 31.1 mEq/L

50Case 2

What is the acid-base disorder?

51Case 2

What is the acid-base disorder?

Recall that for acute respiratory disturbances (where renal compensation does not have much time to occur) each arterial PCO2 shift of 10 mm Hg is accompanied by a pH shift of about 0.08, while for chronic respiratory disturbances (where renal compensation has time to occur) each PCO2 shift of 10 mm Hg is accompanied by a pH shift of about 0.03. 52Case 2

What is the acid-base disorder?

In our case an arterial PCO2 shift of 25 mm Hg (from 40 to 65 mm Hg) is accompanied by a pH shift of 0.10 units (from 7.40 to 7.30), or a 0.04 pH shift for each PCO2 shift of 10 mm. Since 0.04 is reasonably close to the expected value of 0.03 for an chronic respiratory disturbance, it is reasonable to say that the patient has a CHRONIC RESPIRATORY ACIDOSIS. 53Case 2

What is the acid-base disorder?

ANSWER FROM www.medcalc.com/acidbase.html (1) partially compensated primary respiratory acidosis, or (2) acute superimposed on chronic primary respiratory acidosis, or (3) mixed acute respiratory acidosis with a small metabolic alkalosis SAME ANSWER AS IN CASE 1 !! 54Case 3 Patient with Severe Abdominal Pain 55Case 3 Patient with Severe Abdominal PainAn obese 70 year old man has diabetes of 25 years duration complicated by coronary artery disease (CABG x 4 vessels 10 years ago), cerebrovascular disease (carotid artery endarterectomy 3 years ago) and peripheral vascular disease (Aorto-bifem 2 years ago). VASCULOPATH 56Case 3 Patient with Severe Abdominal PainHe now presents to the emergency department with severe, poorly localised abdominal pain with a relatively sudden onset. To the surprise of the intern that examines him, the patient has a relatively normal abdominal examination. Just lots and lots of pain. Nor has the patient had vomiting, diarrhea, or other GI symptoms. 57Case 3 Patient with Severe Abdominal PainThe intern considers the differential diagnosis of severe abdominal pain in the setting of a diabetic vasculopath without much in the way of abdominal signs. She wonders if this might be another manifestation of vascular disease. Following a Google search she finds the following statement at emedicine.com The sine qua non of mesenteric ischemia is a relatively normal abdominal examination in the face of severe abdominal pain. 58Case 3 Patient with Ischemic BowelFollowing discussion with her attending, the patient is to be admitted to a regular nursing floor where he is to be worked up for his abdominal pain. However, he must remain in the emergency department until a bed can be found. When the intern comes by 3 hours later to recheck on the patient he looks much worse. He now has abdominal distention, ileus (no bowel sounds), and signs of shock (BP 75/45). He is rushed to the Intensive Care Unit (ICU). 59Case 3 Patient with Ischemic Bowel 60Burns BJ, Brandt LJ. Intestinal ischemia.Gastroenterol Clin North Am. 2003 Dec32(4)1127-43. Ischemic injury to the gastrointestinal tract can threaten bowel viability with potential catastrophic consequences, including intestinal necrosis and gangrene. The presenting symptoms and signs are relatively nonspecific and diagnosis requires a high index of clinical suspicion. Acute mesenteric ischemia (AMI) often results from an embolus or thrombus within the superior mesenteric artery (SMA), although a low-flow state through an area of profound atherosclerosis may also induce severe ischemia. Because most laboratory and radiologic studies are nonspecific in early ischemia an aggressive approach to diagnosis with imaging of the splanchnic vasculature by mesenteric angiography is advocated. Various therapeutic approaches, including the infusion of vasodilators and thrombolytics, may then be used. Proper diagnosis and management of patients with AMI requires vigilance and a readiness to pursue an aggressive course of action. 61Case 3 Patient with Ischemic Bowel 62Case 3 Patient with Ischemic BowelCLINICAL COMMENTS (emedicine.com) The sine qua non of mesenteric ischemia is a relatively normal abdominal examination in the face of severe abdominal pain. The pain generally is severe and may be relatively refractory to opiate analgesics. Mortality rates of 70-90 have been reported with traditional methods of diagnosis and therapy however, a more aggressive approach may reduce the mortality rate to 45. A survival rate of 90 may be obtained if angiography is obtained prior to the onset of peritonitis. 63Case 3 Patient with Ischemic BowelABGs obtained in the ICU pH 7.18 PCO2 20 mmHg HCO3 7 mEq/L 64Case 3 Patient with Ischemic Bowel 65Case 3 Patient with Ischemic BowelABGs obtained in the ICU pH 7.18 PCO2 20 mmHg HCO3 7 mEq/L 66Case 3 Patient with Ischemic BowelABGs obtained in the ICU pH 7.18 PCO2 20 mmHg HCO3 7 mEq/L What is the primary disorder? What is the physiologic response to this disorder? 67Case 3 Patient with Ischemic BowelStep 1 Acidemic, alkalemic, or normal? Step 2 Is the primary disturbance respiratory or metabolic? Step 3 For a primary respiratory disturbance, is it acute or chronic? Step 4 For a metabolic disturbance, is the respiratory system compensating OK? Step 5 For a metabolic acidosis, is there an increased anion gap? Step 6 For an increased anion gap metabolic acidosis, are there other derangements? 68Case 3 Patient with Ischemic BowelStep 1 Acidemic, alkalemic, or normal? ACIDEMIC 69Case 3 Patient with Ischemic BowelStep 2 Is the primary disturbance respiratory or metabolic? METABOLIC 70Case 3 Patient with Ischemic BowelStep 3 For a primary respiratory disturbance, is it acute or chronic? NOT APPLICABLE 71Case 3 Patient with Ischemic BowelStep 4 For a metabolic disturbance, is the respiratory system compensating OK? DISCUSSION The physiological response to metabolic acidosis is hyperventilation, with a resulting compensatory drop in PCO2 according to "Winter's formula" Expected PCO2 in metabolic acidosis 1.5 x HCO3 8 (range /- 2) If the actual measured PCO2 is much greater than the expected PCO2 from Winter's formula, then the respiratory system is not fully compensating for the metabolic acidosis, and a respiratory acidosis is concurrently present. This may occur, for instance, when respiratory depressants like morphine or fentanyl are administered to the patient to reduce pain. 72Case 3 Patient with Ischemic BowelStep 4 For a metabolic disturbance, is the respiratory system compensating OK? "Winter's formula" Expected PCO2 in metabolic acidosis 1.5 x HCO3 8 (range /- 2) 1.5 x 7 8 18.5 pH 7.18 PCO2 20 mm Hg HOC3 7 mEq / L 73Case 3 Patient with Ischemic BowelStep 5 For a metabolic acidosis, is there an increased anion gap? FOR THIS STEP ONE MUST OBTAIN SERUM ELECTROLYTE DATA 74Case 3 Patient with Ischemic BowelSERUM ELECTROLYTE DATA Serum sodium 135 mEq/L Serum bicarbonate 7 mEq/L Serum chloride 98 mEq/L 75Anion Gap Serum Sodium Serum Chloride Serum Bicarbonate SERUM ELECTROLYTE DATA Serum sodium 135 mEq/L Serum bicarbonate 7 mEq/L Serum chloride 98 mEq/L Anion Gap 135 - 98 -7 mEq/L 30 mEq/L (ELEVATED) 76Case 3 Patient with Ischemic BowelStep 5 For a metabolic acidosis, is there an increased anion gap? ANSWER YES 77Case 3 Patient with Ischemic BowelStep 6 For an increased anion gap metabolic acidosis, are there other derangements? To determine if there are other metabolic derangements present we start by determining the corrected bicarbonate concentration Corrected HCO3 measured HCO3 (Anion Gap - 12). If the corrected HCO3 is less than normal (under 22mEq/L) then there is an additional metabolic acidosis present. Corrected HCO3 values over 26 mEq/L reflect a co-existing metabolic alkalosis. 78Case 3 Patient with Ischemic BowelCorrected HCO3 measured HCO3 (Anion Gap - 12). Corrected HCO3 7 (30 - 12) 25 REMEMBER If the corrected HCO3 is less than normal (under 22mEq/L) then there is an additional metabolic acidosis present. Corrected HCO3 values over 26 mEq/L reflect a co-existing metabolic alkalosis. 79Case 3 Patient with Ischemic BowelStep 6 For an increased anion gap metabolic acidosis, are there other derangements? ANSWER NO OTHER DERANGEMENTS NOTED 80Case 3 Patient with Ischemic BowelANSWER FROM www.medcalc.com/acidbase.html Primary metabolic acidosis, with increased anion gap, with full respiratory compensation 81Case 3 Patient with Ischemic BowelBUT What is the cause of the elevated anion-gap metabolic acidosis? 82Case 3 Patient with Ischemic BowelThe most common etiologies of a metabolic acidosis with an increased anion gap are shown below ? Lactic acidosis ? Ingestion of (from poor perfusion) ? Ethylene glycol? Starvation ? Methanol? Renal failure ? Salicylate? Ketoacidosis (as in diabetic ketoacidosis) 83Notes on Lactic Acidosis Lactic acidosis is a disease characterized by a pH less than 7.25 and a plasma lactate greater than 5 mmol/L. Hyperlactemia results from abnormal conversion of pyruvate into lactate. Lactic acidosis results from an increase in blood lactate levels when body buffer systems are overcome. This occurs when tissue oxygenation is inadequate to meet energy and oxygen need as a result of either hypoperfusion or hypoxia. emedicine.com

A 52-year-old man with Hodgkin's disease is treated with ABVD, a combination chemotherapy regimen. Unfortunately, despite treatment with antiemetics, he suffers from severe, persistent vomiting. When seen by his physician, he is dehydrated and has shallow respirations.

The pH of the arterial blood gas identifies it as alkalemic. (Recall that the normal range for arterial blood pH is 7.35 to 7.45).

103

Step 2 Is the primary disturbance respiratory or metabolic?

The primary disturbance is metabolic, with the HCO3 being elevated. Since the PCO2 is raised in the face of an alkalemia, there is obviously not a primary respiratory disturbance the raised PCO2 merely indicates that respiratory compensation has occurred.

104Step 3 Not applicable in this case. 105

Step 4 The expected PCO2 in metabolic alkalosis is 0.7 x HCO3 20 mmHg 0.7 x 45 20 52 mm Hg. Since the actual PCO2 (54) and the expected PCO2 (52) are approximately the same, this suggests that respiratory compensation is appropriate.

106Steps 5-7 Not applicable in this case. 107Case 4 108DIAGNOSIS Metabolic Alkalosis from Persistent Vomiting due to Chemotherapy. 109What About the Low Potassium?

pH 7.56

PCO2 54 mm Hg

BUN 52 mg/dl (NL7 18)

Creatinine 1.8 mg/dl (NL0.7 1.2)

K 2.8 mEq/l

HCO3 45 mmol/l

110

111

112Medical News Summary Woman allegedly dies of potassium overdose in hospital Date 10 October 2004 Source Canada Press Author Michelle Macafee Medical News Summary (summary of medical news story as reported by Canada Press) An 83 year old woman allegedly died after her IV pump was set at double the required speed. The nurse only became aware of the error after the patient died. An autopsy showed she died from a heart attack induced by potassium overdose. The case is being investigated. URL http//www.canada.com/health/story.html?id6c6d5a12-3d33-4c42-baa3-4826f0d25a9d

114Case 5A 31 year old man presents with lethargy, weakness, labored respiration, and confusion. He has had diabetes for 15 years, and has been suffering from the intestinal flu for a day or so, for which he has been avoiding food to help prevent further vomiting and make his stomach ache go away. Since he stopped eating, he thought that it would be a good idea to stop taking his insulin. When seen in the emergency department his urine dipped positive for both glucose and ketones and his breath had a strange sweet, fruity smell. 115

The following arterial blood gas data is obtained

pH 7.27

PCO2 23 mm Hg

Na 132 mEq/L

Cl - 83 mEq/L

K 4.9 mEq/L

HCO3 10 mEq/L

Glucose 345 mg/dL

116Case 5 117Steps

Step 1. The pH is 7.27, which is considerably less than normal (7.35-7.45), so the patient is acidemic.

Step 2 The PCO2 is low, so the respiratory system is not causing the acidosis rather, the drop in PCO2 must be a compensatory process. The bicarbonate is low, which indicates that a metabolic acidosis is present.

Step 3 Not applicable in this case.

118Steps

Step 4 According to "Winter's formula" the expected PCO2 in metabolic acidosis is 1.5 x HCO3 8 1.5 x 10 8 23 mm Hg. Since the actual and expected PCO2 are the same, this suggests that the respiratory compensation is appropriate.

Step 6 Remember that corrected HCO3 measured HCO3 (anion gap - 12). In this case the corrected HCO3 10 (39 12) 37. The corrected HCO3 is much higher than a normal HCO3, suggesting there is a concurrent metabolic alkalosis, likely as a result of persistent vomiting.

121Case 6 Pregnant Woman with Persistent Vomiting 122Case 6 Pregnant Woman with Persistent VomitingA 23-year-old woman is 12 weeks pregnant. For the last with 10 days she has had worsening nausea and vomiting. When seen by her physician, she is dehydrated and has shallow respirations. Arterial blood gas data is as follows pH 7.56 PCO2 54 mm Hg 123Step 1 Acidemic, alkalemic, or normal? Step 2 Is the primary disturbance respiratory or metabolic? Step 3 For a primary respiratory disturbance, is it acute or chronic? Step 4 For a metabolic disturbance, is the respiratory system compensating OK? Step 5 For a metabolic acidosis, is there an increased anion gap? Step 6 For an increased anion gap metabolic acidosis, are there other derangements? 124Step 1 Acidemic, alkalemic, or normal? The pH of the arterial blood gas identifies it as alkalemic. (Recall that the normal range for arterial blood pH is 7.35 to 7.45). 125 Step 2 Is the primary disturbance respiratory or metabolic? The primary disturbance is metabolic, with the HCO3 being elevated. Since the PCO2 is raised in the face of an alkalemia, there is obviously not a primary respiratory disturbance the raised PCO2 merely indicates that respiratory compensation has occurred. 126 Step 3 For a primary respiratory disturbance, is it acute or chronic? Not applicable in this case. 127 Step 4 For a metabolic disturbance, is the respiratory system compensating OK? The expected PCO2 in metabolic alkalosis is 0.7 x HCO3 20 mmHg 0.7 x 45 20 52 mm Hg. Since the actual PCO2 (54) and the expected PCO2 (52) are approximately the same, this suggests that respiratory compensation is appropriate. 128 Step 5 For a metabolic acidosis, is there an increased anion gap? Not applicable in this case. 129 Step 6 For an increased anion gap metabolic acidosis, are there other derangements? Not applicable in this case. 130 pH 7.56 PCO2 54 mm Hg DIAGNOSIS Metabolic Alkalosis from Persistent Vomiting 131 DIAGNOSIS Metabolic Alkalosis from Persistent Vomiting 132 Metabolic Alkalosis from Persistent Vomiting 133(No Transcript) 134MERTABOLIC ALKALOSISMetabolic alkalosis is a primary increase in serum bicarbonate (HCO3-) concentration. This occurs as a consequence of a loss of H from the body or a gain in HCO3-. In its pure form, it manifests as alkalemia (pH gt7.40). As a compensatory mechanism, metabolic alkalosis leads to alveolar hypoventilation with a rise in arterial carbon dioxide tension (PaCO2), which diminishes the change in pH that would otherwise occur. emedicine.com 135Nausea and vomiting in pregnancy is extremely common. Studies estimate nausea occurs in 66-89 of pregnancies and vomiting in 38-57. The nausea and vomiting associated with pregnancy almost always begins by 9-10 weeks of gestation, peaks at 11-13 weeks, and resolves (in 50 of cases) by 12-14 weeks. In 1-10 of pregnancies, symptoms may continue beyond 20-22 weeks. The most severe form of nausea and vomiting in pregnancy is called hyperemesis gravidarum (HEG). HEG is characterized by persistent nausea and vomiting associated with ketosis and weight loss (gt5 of prepregnancy weight). HEG may cause volume depletion, altered electrolytes, and even death. emedicine.com 136Charlotte Bronte, the famous 19th century author of Jane Eyre, died of hyperemesis in 1855 in her fourth month of pregnancy. 137Case 7 Expedition to the Top of Mount Everest 138(No Transcript) 139The atmospheric pressure at the summit of Mount Everest (29,028') is about a third that at sea level. When an ascent is made without oxygen, extreme hyperventilation is needed if there is to be any oxygen at all in the arterial blood (a direct consequence of the alveolar gas equation). Typical summit data (West 1983) pH 7.7 PCO2 7.5 140West JB, Hackett PH, Maret KH, Milledge JS, Peters RM Jr, Pizzo CJ, Winslow RM. Pulmonary gas exchange on the summit of Mount Everest.J Appl Physiol. 1983 Sep55(3)678-87. Pulmonary gas exchange was studied on members of the American Medical Research Expedition to Everest at altitudes of 8,050 m (barometric pressure 284 Torr), 8,400 m (267 Torr) and 8,848 m (summit of Mt. Everest, 253 Torr). Thirty-four valid alveolar gas samples were taken using a special automatic sampler including 4 samples on the summit. Venous blood was collected from two subjects at an altitude of 8,050 m on the morning after their successful summit climb. Alveolar CO2 partial pressure (PCO2) fell approximately linearly with decreasing barometric pressure to a value of 7.5 Torr on the summit. For a respiratory exchange ratio of 0.85, this gave an alveolar O2 partial pressure (PO2) of 35 Torr. In two subjects who reached the summit, the mean base excess at 8,050 m was -7.2 meq/l, and assuming the same value on the previous day, the arterial pH on the summit was over 7.7. Arterial PO2 was calculated from changes along the pulmonary capillary to be 28 Torr. In spite of the severe arterial hypoxemia, high pH, and extremely low PCO2, subjects on the summit were able to perform simple tasks. The results allow us to construct for the first time an integrated picture of human gas exchange at the highest point on earth. 141(No Transcript) 142(No Transcript) 143Case 8 Patient with a Subarachnoid Hemorrhage (Patient of Dr. M. Lotto, January 2006) 40154388 144

A 22-year-old man was severely injured in the chest from a motor vehicle accident. A large flail rib segment in his thorax is compromising his breathing. A blood gas sample was taken, revealing the following

pH 7.21

PCO2 65

HCO3 25

149A flail chest segment moves paradoxically (in an opposite direction from the rest of the ribs) and impairs ventilation as a result. The result is hypoventilation. Image Credit tooldoc.wncc.nevada.edu /breath8.JPG 150

Step 1 Acidemic, alkalemic, or normal?

The pH of the arterial blood gas identifies it as acidemic. (Recall that the normal range for arterial blood pH is 7.35 to 7.45).

Step 2 Is the primary disturbance respiratory or metabolic?

The primary disturbance is respiratory, with the PCO2 being significantly elevated. Since the bicarbonate is normal, there is no primary metabolic disturbance. (Recall that that the normal range for arterial PCO2 is 35- 45 mm Hg).

151

Step 3 For a respiratory disturbance, is it acute or chronic?

Recall that for acute respiratory disturbances (where renal compensation does not have much time to occur) each arterial PCO2 shift of 10 mm Hg is accompanied by a pH shift of 0.08, while for chronic respiratory disturbances (where renal compensation has time to occur) each PCO2 shift of 10 mm Hg is accompanied by a pH shift of 0.03.

In our case an arterial PCO2 shift of 25 mm Hg is accompanied by a pH shift of 0.19 units, or about a 0.08 pH shift for each PCO2 shift of 10 mm. This means that the respiratory disturbance is acute. (If it were chronic the pH shift would be 0.003 x 25 0.075, for a resulting pH of 7.4 0.12 7.33).

A 39-year-old woman had severe chronic back pain, which she treated aggressively with a variety of OTC Non Steroidal Anti-Inflammatory Drugs (NSAIDs) for a number of years. At a routine clinical visit her blood pressure is found to be elevated at 155/95. Her urine dips 2 positive for protein, and microscopic examination of her urine reveals 4-5 white blood cells per high-power field (4-5 WBC / hpf) with a specific gravity of 1.01 and a pH of 5.0.

155

An arterial blood gas sample is as follows

pH 7.30

PCO2 32 mm Hg

HCO3 15 mEq/L

Na 138 mEq/L

K 5.1 mEq/L

Cl 111 mEq/L

156

Step 1 Acidemic, alkalemic, or normal?

The pH is 7.30, which is far less than normal (7.35-7.45), so the patient is acidemic.

Step 2 Is the primary disturbance respiratory or metabolic?

The PCO2 is low, so the respiratory system is not causing the acidosis rather, the drop in PCO2 must be a compensatory process. The bicarbonate is low, which indicates that a metabolic acidosis is present.

Step 3 Not applicable in this case.

157

Step 4 According to "Winter's formula" the expected PCO2 in metabolic acidosis is 1.5 x HCO3 8 1.5 x 15 8 31 mm Hg. Since the actual and expected PCO2 are approximately the same, this suggests that the respiratory compensation is appropriate.

Step 7 Urinary electrolytes are needed to determine the urinary anion gap, but are unavailable here. On clinical grounds one would expect a renal rather than GI cause for her normal anion gap metabolic acidosis.

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